Fig. 1. Peripheral blood neutrophils from IL8Rh (+/+) and (-/-) mice derived under SPF and GF conditions. Blood was collected by retroorbital venous puncture and was analyzed in a Serono-Baker Diag-nostics System 9000 Diff Model Hematology Analyzer. Blood smears were stained with hematoxylin and eosin for differential cell counts per-formed microscopically. The total number of neutrophils was determined by multiplying the percentage of neutrophils by total white cell counts. Bars represent individual mice. and periodontal disease are also observed with LAD type II where 32-integrin expression is normal, but neutrophils have altered L-selec-tin expression and reducedefficiency to egress into tissues (6). Our experience with LAD cattle suggests that cytokine and chemoattrac-tant production by tissues encountering nor-mal flora or pathogens is not effectively downregulated, as theeliciting agents are not re-moved by normal inflammatory processes. Not down-regulating inflammatory cytokine production (for example, granulocyte-macrophage colony-stimulatory factor) in infected tissues could be expected to result in the observed histopathological changes in the host, such as a progressiveneutrophilia. In support of this hypothesis, the neutrophilia is much lower in LAD animals raised under germ-free conditions (3) than they are in animals raised conventionally. The work of Cacalano et al. shows that mice lacking the mIL-8Rh, like LAD patients, suffer a marked impairment in neu-trophil recruitment, and the hematological and histological changes in these mice are nearly identical to those associated with LAD. Furthermore, some of these mice suffer growth retardation and abnormal denti-tion (7). Together, these data suggest that a severe impairment to neutrophil recruitment, whether through absence of adhesion molecules or chemoattractant receptors, reduc-es host defense to normal bacterial exposure and leads to compensatory changes in the immune system. This conclusion leads to the more significant implication that ligands of the mIL-8Rh must be essential for the surveillance function of neutrophils, at least in mice. Apparently, none of the other neutrophil chemoattractants-for example, leukotriene B4, complement fragments, or bacterial products-enable adequate neutrophil recruitment for normal host defense in the absence of the mIL-8Rh. Dale E. Shuster